High accuracy ranging for space debris with spaceborne single photon Lidar.

The increasing risk posed by space debris highlights the need for accurate localization techniques. Spaceborne single photon Lidar (SSPL) offers a promising solution, overcoming the limitations of traditional ground-based systems by providing expansive coverage and superior maneuverability without being hindered by weather, time, or geographic constraints. This study introduces a novel approach leveraging non-parametric Bayesian inference and the Dirichlet process mixture model (DPMM) to accurately determine the distance of space debris in low Earth orbit (LEO), where debris exhibits nonlinear, high dynamic motion characteristics. By integrating extended Kalman filtering (EKF) for range gating, our method captures the temporal distribution of reflected photons, employing Markov chain Monte Carlo (MCMC) for iterative solutions. Experimental outcomes demonstrate our method's superior accuracy over conventional statistical techniques, establishing a clear correlation between radial absolute velocity and ranging error, thus significantly enhancing monostatic space debris localization.

Underwater single photon 3D imaging with millimeter depth accuracy and reduced blind range.

Mono-static system benefits from its more flexible field of view and simplified structure, however, the backreflection photons from mono-static system lead to count loss for target detection. Counting loss engender range-blind, impeding the accurate acquisition of target depth. In this paper, count loss is reduced by introducing a polarization-based underwater mono-static single-photon imaging method, and hence reduced blind range. The proposed method exploits the polarization characteristic of light to effectively reduce the count loss of the target, thus improving the target detection efficiency. Experiments demonstrate that the target profile can be visually identified under our method, while the unpolarization system can not. Moreover, the ranging precision of system reaches millimeter-level. Finally, the target profile is reconstructed using non-local pixel correlations algorithm.

Osthole inhibits GSK-3ß/AMPK/mTOR pathway-controlled glycolysis and increases radiosensitivity of subcutaneous transplanted hepatocellular carcinoma in nude mice.

PURPOSE: Osthole possesses anti-tumor activities. However, whether osthole can have a radiosensitization effect on hepatic cancer remains unclear. Here, an HCC-LM3 cells-inoculated subcutaneous transplanted tumor was adopted to explore the effect of osthole. METHODS: The tumor-bearing mice were treated with 100 mg/kg osthole for 12 days, 4 Gy irradiation twice, or their combination. The tumor volume and weight, lactic acid content, glycolytic enzyme activities, and protein expression of glycogen synthase kinase 3ß (GSK-3ß), p­GSK-3ß, mammalian target of rapamycin (mTOR), p­mTOR, AMP-activated protein kinase (AMPK), p­AMPK, glucose transporter 1/3, and pyruvate kinase M2 were determined. The GSK-3ß-overexpressed HCC-LM3 or SK-Hep­1 cell models were also adopted to verify the effects of osthole on expression of these proteins. RESULTS: The tumor volume and weight, lactic acid content, and glycolytic enzyme activities in tumor tissues were lower in the osthole + radiation group than in the radiation group. Moreover, osthole could reverse the radiation-induced increments of p­GSK-3ß/GSK-3ß and p­mTOR/mTOR protein ratios and the expression of glucose transporter 1/3 and pyruvate kinase M2 proteins in tumor tissues, and increase the protein ratio of p­AMPK/AMPK. The effects of osthole on these glycolysis-related proteins were also observed in GSK-3ß-overexpressed HCC-LM3 or SK-Hep­1 cell models. CONCLUSION: Osthole has a radiosensitizing effect on subcutaneous transplanted hepatocellular carcinoma, and its mechanism may be related to inhibition of GSK-3ß/AMPK/mTOR pathway-controlled glycolysis.

On-orbit space optical communication demonstration with a 22†s acquisition time.

The inherent small divergence angle of space optical communication poses significant challenges to establishing communication links. Therefore, laser link acquisition becomes a crucial technology in optical communication, with a primary focus on reducing the acquisition time effectively. Conventional optical communication acquisition techniques fail to address the error effects caused by satellite insertion into the Earth orbit, thus unable to meet the rapid establishment demands of laser links in satellite optical communication networks. In this regard, we propose a novel, to the best of our knowledge, on-orbit calibration method for laser communication terminals to our knowledge. Leveraging stellar observations, this method achieves efficient on-orbit calibration with only a single observation. Theoretical analysis and on-orbit experimental results demonstrate that this approach effectively enhances an open-loop pointing accuracy, offering promising prospects for achieving a rapid establishment of optical communication links in ultra-long-distance optical communication missions.

Osthole Increases the Sensitivity of Liver Cancer to Sorafenib by Inhibiting Cholesterol Metabolism.

Osthole is a natural product that has an inhibitory effect on liver cancer, but its effect on the sensitivity of liver cancer to sorafenib is poorly understood. Here, we investigated the effect of osthole and possible sensitization mechanisms. Our results showed that the combination of 2.5 µM sorafenib and 10 µM osthole had significantly synergistic inhibitory effects on proliferation, colony formation, and migration of HCCLM3, sorafenib-resistant HCCLM3 (HCCLM3-SR), and SK-Hep-1 cells. After treatment of HCCLM3 cells-inoculated subcutaneous xenotransplanted tumor mice with 100 mg/kg osthole, 70 mg/kg sorafenib or their combination for 24 day, the tumor volume, tumor weight, and tumor weight coefficient were significantly lower in the osthole + sorafenib group than in the sorafenib group. Compared with the control group, the total cholesterol and low density lipoprotein-cholesterol contents in serum and tumor tissue were significantly decreased in the osthole or osthole + sorafenib groups, the sterol regulatory element binding protein (SREBP)-2c, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), and low-density lipoprotein receptor (LDLR) protein expressions in tumor tissue were significantly downregulated as well. In conclusion, osthole can increase the sensitivity of liver cancer to sorafenib, and the mechanism is related to the downregulations of SREBP-2c, HMGCR, and LDLR protein expressions and subsequent inhibition of cholesterol metabolism.

Stevioside inhibits lipopolysaccharide-induced epithelial-to-mesenchymal transition of NRK-52E cells by PPARγ activation.

BACKGROUND: Stevioside is a natural diterpenoid compound that possesses anti-inflammatory, immunomodulatory, anti-diabetic, anti-hypertensive, and renal protective effects, but its effect on lipopolysaccharide (LPS)-induced epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells, an important immune pathological mechanism of renal fibrosis, remains unknown. This study employed the renal proximal tubular cells NRK-52E to investigate the effect of stevioside. METHODS: The LPS-stimulated renal NRK-52E cells were treated with 50, 100, or 200 µM stevioside in the presence or absence of peroxisome proliferator-activated receptor γ (PPARγ) antagonist GW9662, the expression levels of intracellular E-cadherin, vimentin, α-smooth muscle actin (α-SMA), PPARγ, nuclear factor kappa B (NF-κB) p65, transforming growth factor-ß1 (TGF-ß1), signal transducer and activator of transcription 3 (STAT3), p-STAT3, Smad2/3, and p-Smad2/3 proteins were detected by Western blot analysis. RESULTS: In LPS-stimulated NRK-52E cells, stevioside treatment could reverse the expressions of EMT-related E-cadherin, vimentin, and α-SMA proteins, increase the expression of PPARγ protein, and decrease the expressions of NF-κB p65, TGF-ß1, p-STAT3, Smad2/3, and p-Smad2/3 proteins, especially in the 200 µM stevioside-treated group. However, these beneficial effects of stevioside were attenuated or canceled by pretreatment with PPARγ antagonist GW9662. CONCLUSIONS: Stevioside can inhibit the LPS-induced EMT via the reductions of NF-κB, TGF-ß1, Smad2/3, p-Smad2/3, and p-STAT3 protein expressions by PPARγ activation in NRK-52E cells, which may provide a pharmacological basis for the potential application of stevioside in the prevention and treatment of renal fibrosis.

Apigenin inhibits isoproterenol-induced myocardial fibrosis and Smad pathway in mice by regulating oxidative stress and miR-122-5p/155-5p expressions.

Apigenin, a flavonoid isolated from Apium graveolens, is an effective natural active ingredient that inhibits transforming growth factor-ß1 (TGF-ß1)-induced cardiac fibroblasts (CFs) differentiation and collagen synthesis. However, its effects on isoproterenol-induced myocardial fibrosis in mice remain unknown. This study aimed to examine the effect of apigenin in the prevention of myocardial fibrosis. A mouse model of myocardial fibrosis induced by isoproterenol was established, and the mice were given apigenin 75-300 mg/kg orally for 40 days. The results showed that the heart weight coefficient, myocardial hydroxyproline, collagen accumulation, and malondialdehyde levels in the apigenin-treated groups were significantly reduced. In contrast, the activity of myocardial superoxide dismutase and glutathione peroxidase were significantly enhanced. The results of real-time quantitative polymerase chain reaction and western blot assays showed that apigenin could significantly upregulate the expressions of myocardial microRNA-122-5p (miR-122-5p), c-Ski, and Smad7 and downregulate the expressions of myocardial miR-155-5p, α-smooth muscle actin, collagen I/III, NF-κB, TGF-ß1, hypoxia-inducible factor-1α (HIF-1α), Smad2/3, and p-Smad2/3. In vitro, the differentiation and extracellular matrix production, as well as TGF-ß1/Smads axis, were further reduced after treatment of miR-122-5p mimic or miR-155-5p inhibitor-transfected and TGF-ß1-stimulated CFs with apigenin. These results suggested that apigenin increased the expression of miR-122-5p and decreased the expression of miR-155-5p, which subsequently downregulated and upregulated the target genes HIF-1α and c-Ski, respectively. Furthermore, apigenin administration downregulated TGF-ß1-induced Smad2/3 and upregulated Smad7. In addition, it reduced the NF-κB/TGF-ß1 signaling pathway axis by increasing antioxidant ability to exert the antifibrotic effects.

Carbon Nanolights in Piezopolymers are Self-Organizing Toward Color Tunable Luminous Hybrids for Kinetic Energy Harvesting.

Herein, an all-solid-state sequential self-organization and self-assembly process is reported for the in situ construction of a color tunable luminous inorganic/polymer hybrid with high direct piezoresponse. The primary inorganic self-organization in solid polymer and the subsequent polymer self-assembly are achieved at high pressure with the first utilization of piezo-copolymer (PVDF-TrFE) as the host matrix of guest carbon quantum dots (CQDs). This process induces the spontaneous formation of a highly ordered, microscale, polygonal, and hierarchically structured CQDs/PVDF-TrFE hybrid with multicolor photoluminescence, consisting of very thermodynamic stable polar crystalline nanowire arrays. The electrical polarization-free CQDs/PVDF-TrFE hybrids can efficiently harvest the environmental available kinetic mechanical energy with a new large-scale group-cooperation mechanism. The open-circuit voltage and short-circuit current outputs reach up to 29.6 V cm-2 and 550 nA cm-2 , respectively. The CQDs/PVDF-TrFE-based hybrid nanogenerator demonstrates drastically improved durable and reliable features during the real-time demonstration of powering commercial light emitting diodes. No attenuation/fluctuation of the electrical signals is observed for ≈10 000 continuous working cycles. This study may offer a new design concept for progressively but spontaneously constructing novel multiple self-adaptive complex inorganic/polymer hybrids that promise applications in the next generation of self-powered autonomous optoelectronic devices.

Aqueous Phase Exfoliating Quasi-2D CsPbBr3 Nanosheets with Ultrahigh Intrinsic Water Stability.

All-inorganic cesium lead halide perovskite nanocrystals (NCs) have emerged as attractive optoelectronic materials due to the excellent optical and electronic properties. However, their environmental stability, especially in the presence of water, is still a significant challenge for their further commercialization. Here, ultrahigh intrinsically water-stable all-inorganic quasi-2D CsPbBr3 nanosheets (NSs) via aqueous phase exfoliation method are reported. Compared to conventional perovskite NCs, these unique quasi-2D CsPbBr3 nanosheets present an outstanding long-term water stability with 87% photoluminescence (PL) intensity remaining after 168 h under water conditions. Moreover, the photoluminescence quantum yields (PLQY) of quasi-2D CsPbBr3 NSs is up to 82.3%, and these quasi-2D CsPbBr3 NSs also present good photostability of keeping 85% PL intensity after 2 h under 365 nm UV light. Evidently, such quasi-2D perovskite NSs will open up a new way to investigate the intrinsic stability of all-inorganic perovskites and further promote the commercial development of perovskite-based optoelectronic and photovoltaic devices.

Structural and Optical Investigations of Quasi-Single Crystal Eu3+-Doped BaWO4 Thin Films.

Scheelite-structure tungstates with unique structural features and excellent luminescence possess promising applications, such as light-emitting diodes (LEDs), scintillators, and displays. The controllable growth of high quality and uniform composition thin films mounted on cheap substrates is a key factor to realize the above commercial applications, however, which is also a big challenge due to the difficult stress release stemming from intrinsic lattice mismatches. Here, we employed the simple and composition-controlled polymer-assisted deposition (PAD) method to successfully obtain a series of high quality and well-proportioned BaWO4:Eu3+ (BWOE) thin films with red emission. Screening out the unbound freedom metal ions by poly(ether imide) (PEI) and ethylene diamine tetraacetic acid (EDTA), the firmly bound metal ions (Ba2+, W6+ and Eu3+) in polymer solution were applied to accurately control the chemical composition and effectively governed the release of stress during the growth process of BWOE thin films. Furthermore, XRD, SEM and EDS mapping detections evidently authenticated the quasi-single crystallinity, uniform morphology and well-distributed composition of as-grown thin films. Additionally, excited by 250 nm light, these thin films could efficiently produce the red emission, peaked at around 612 nm originated from the 5 D0 → 7 F2 transition of Eu3+. Moreover, the optimal doping concentration of thin films was confirmed to be 9% and corresponding Commission International de l'Eclairage (CIE) chromaticity coordinate was (0.618, 0.365), which evidently implied the excellent color rending index. Therefore, this work highlights the rather superior PAD method to prepare uniform and high-quality BWOE thin films, which can be expanded toward the other photoelectric devices including white lighted-emitting diodes, scintillators, displays, and photoelectric detectors.

PPARα/γ antagonists reverse the ameliorative effects of osthole on hepatic lipid metabolism and inflammatory response in steatohepatitic rats.

Our previous studies have indicated that osthole may ameliorate the hepatic lipid metabolism and inflammatory response in nonalcoholic steatohepatitic rats, but the underlying mechanisms remain unclear. This study aimed to determine whether the effects of osthole were mediated by the activation of hepatic peroxisome proliferator-activated receptor α/γ (PPARα/γ). A rat model with steatohepatitis was induced by orally feeding high-fat and high-sucrose emulsion for 6 weeks. These experimental rats were then treated with osthole (20 mg/kg), PPARα antagonist MK886 (1 mg/kg) plus osthole (20 mg/kg), PPARγ antagonist GW9662 (1 mg/kg) plus osthole (20 mg/kg) and MK886 (1 mg/kg) plus GW9662 (1 mg/kg) plus osthole (20 mg/kg) for 4 weeks. The results showed that after osthole treatment, the hepatic triglycerides, free fatty acids, tumor necrosis factor-α, monocyte chemotactic protein-1, interleukin-6 (IL-6), IL-8 and liver index decreased by 52.3, 31.0, 32.4, 28.9, 36.3, 29.3 and 29.9%, respectively, and the score of steatohepatitis also decreased by 70.0%, indicating that osthole improved the hepatic steatosis and inflammation. However, these effects of osthole were reduced or abrogated after simultaneous addition of the specific PPARα antagonist MK886 or/and the PPARγ antagonist GW9662, especially in the co-PPARα/γ antagonists-treated group. Importantly, the osthole-induced hepatic expressions of PPARα/γ proteins were decreased, and the osthole-regulated hepatic expressions of lipogenic and inflammatory gene proteins were also reversed by PPARα/γ antagonist treatment. These findings demonstrated that the ameliorative effect of osthole on nonalcoholic steatohepatitis was mediated by PPARα/γ activation, and osthole might be a natural dual PPARα/γ activator.

Apigenin inhibits d-galactosamine/LPS-induced liver injury through upregulation of hepatic Nrf-2 and PPARγ expressions in mice.

Apigenin is a natural flavonoid compound widely distributed in a variety of vegetables, medicinal plants and health foods. This study aimed to examine the protective effect of apigenin against d-galactosamine (D-GalN)/lipopolysaccharide (LPS)-induced mouse liver injury and to investigate the potential biochemical mechanisms. The results showed that after oral administration of apigenin 100-200 mg/kg for 7 days, the levels of serum alanine aminotransferase and aspartate aminotransferase were decreased, and the severity of liver injury was alleviated. Importantly, apigenin pretreatment increased the levels of hepatic nuclear factor erythroid 2-related factor 2 (Nrf-2) and peroxisome proliferator-activated receptor γ (PPARγ) protein expressions as well as superoxide dismutase, catalase, glutathione S-transferase and glutathione reductase activities, decreased the levels of hepatic nuclear factor-κB (NF-κB) protein expression and tumor necrosis factor-α. These findings demonstrated that apigenin could prevent the D-GalN/LPS-induced liver injury in mice, and its mechanisms might be associated with the increments of Nrf-2-mediated antioxidative enzymes and modulation of PPARγ/NF-κB-mediated inflammation.

Osthole improves glucose and lipid metabolism via modulation of PPARα/γ-mediated target gene expression in liver, adipose tissue, and skeletal muscle in fatty liver rats.

CONTEXT: Osthole may be a dual agonist of peroxisome proliferator-activated receptors (PPAR) α/γ and ameliorate the insulin resistance (IR), but its mechanisms are not yet understood completely. OBJECTIVE: We investigated the effects of osthole on PPARα/γ-mediated target genes involved in glucose and lipid metabolism in liver, adipose tissue, and skeletal muscle in fatty liver and IR rats. MATERIALS AND METHODS: The rat model was established by orally feeding high-fat and high-sucrose emulsion for 9 weeks. The experimental rats were treated with osthole 5-10 mg/kg by gavage after feeding the emulsion for 6 weeks, and were sacrificed 4 weeks after administration. RESULTS: After treatment with osthole 5-10 mg/kg for 4 weeks, the lipid levels in serum and liver were decreased by 37.9-67.2% and 31.4-38.5% for triglyceride, 33.1-47.5% and 28.5-31.2% for free fatty acid, respectively, the fasting blood glucose, fasting serum insulin, and homeostasis model assessment of IR were also decreased by 17.2-22.7%, 25.9-26.7%, and 37.5-42.8%, respectively. Osthole treatment might simultaneously decrease the sterol regulatory element binding protein-1c, diacylglycerol acyltransferase, and fatty acid synthase mRNA expressions in liver and adipose tissue, and increase the carnitine palmitoyltransferase-1A mRNA expression in liver and glucose transporter-4 mRNA expression in skeletal muscle, especially in the osthole 10 mg/kg group (p < 0.01). DISCUSSION AND CONCLUSION: Osthole can improve glucose and lipid metabolism in fatty liver and IR rats, and its mechanisms may be associated with synergic modulation of PPARα/γ-mediated target genes involved in glucose and lipid metabolism in liver, adipose tissue, and skeletal muscle.

Chrysanthemum morifolium extract improves hypertension-induced cardiac hypertrophy in rats by reduction of blood pressure and inhibition of myocardial hypoxia inducible factor-1alpha expression.

CONTEXT: Chrysanthemum morifolium Ramat. (Asteraceae) extract (CME) possesses a vasodilator effect in vitro. However, the use of polyphenol-rich CME in the treatment of hypertension-induced cardiac hypertrophy has not been reported. OBJECTIVE: We investigated the effect of polyphenol-rich CME on hypertension-induced cardiac hypertrophy in rats and its possible mechanism of action. MATERIALS AND METHODS: The Sprague-Dawley rat model with cardiac hypertrophy was induced by renovascular hypertension. The blood pressure, cardiac weight index, free fatty acids (FFA) in serum and myocardium, and protein expressions of myocardial hypoxia inducible factor-1α (HIF-1α), peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyltransferase-1a (CPT-1a), pyruvate dehydrogenase kinase-4 (PDK-4) and glucose transporter-4 (GLUT-4) were measured after treating hypertensive rats with polyphenol-rich CME of anthodia 75-150 mg/kg once daily for 4 weeks. A myocardial histological examination was also conducted. RESULTS: After CME treatment, the blood pressure, cardiac weight and cardiac weight index decreased by 5.7-9.6%, 9.2-18.4% and 10.9-20.1%, respectively, and the cardiomyocyte cross-sectional area also decreased by 8.3-30.4%. The CME treatment simultaneously decreased the FFA in serum and myocardium and protein expressions of myocardial HIF-1α and GLUT-4, and increased the protein expressions of myocardial PPARα, CPT-1a and PDK-4, especially in the CME 150 mg/kg group (p < 0.05 or p < 0.01). DISCUSSION AND CONCLUSION: Polyphenol-rich CME may alleviate hypertensive cardiac hypertrophy in rats. Its mechanisms may be related to the reduction of blood pressure and amelioration of the myocardial energy metabolism. The latter may be attributed to the inhibition of HIF-1α expression and subsequent modulation of PPARα-mediated CPT-1a, PDK-4 and GLUT-4 expressions.

PPARα/γ agonists and antagonists differently affect hepatic lipid metabolism, oxidative stress and inflammatory cytokine production in steatohepatitic rats.

Peroxisome proliferator-activated receptor (PPAR) α/γ may control lipid metabolism and inflammatory response by regulating the downstream target genes, and play a crucial role in the process of non-alcoholic steatohepatitis (NASH) formation, but the difference and interaction between PPARα and PPARγ are poorly understood. The rat model with NASH was established by orally feeding high-fat and high-sucrose emulsion for 6weeks. The results shown that after the model rats were simultaneously treated with PPARα/γ agonists, the total cholesterol (TC), triglyceride (TG) and inflammatory cytokine levels in serum and hepatic tissue, the hepatic steatosis and inflammatory cellular infiltration were decreased, and were consistent with the results of hepatic lipogenic gene and nuclear factor (NF)-κB protein expressions. Conversely, these indexes were increased by PPARα/γ antagonist treatment. Compared with the model group, the serum free fatty acid (FFA) level was increased in the PPARα agonist-treated group, decreased in the PPARγ agonist-treated group, and unchanged in the PPARα/γ agonists-treated group. The hepatic FFA level was low in the PPARα/γ agonists-treated groups, but no significant variation in the PPARα/γ antagonists-treated groups. The increments of hepatic reduced glutathione (GSH) and superoxide dismutase (SOD) contents in the PPARα/γ agonists-treated groups were accompanied by decreased hepatic malondialdehyde (MDA) content. These findings demonstrated that PPARα/γ activation might decrease the hepatic lipid accumulation, oxidative stress and inflammatory cytokine production, and PPARγ could counterbalance the adverse effect of PPARα on circulating FFA. It was concluded that the integrative application of PPARα and PPARγ agonists might exert a synergic inhibitory effect on NASH formation through the modulation of PPARα/γ-mediated lipogenic and inflammatory gene expressions.

Osthole inhibits inflammatory cytokine release through PPARα/γ-mediated mechanisms in LPS-stimulated 3T3-L1 adipocytes.

CONTEXT: Peroxisome proliferator-activated receptor (PPAR) α/γ may control inflammatory response by regulating the nuclear factor-kappa B (NF-κB). Osthole may be a dual agonist of PPARα/γ, but whether or not osthole may inhibit inflammatory cytokines in cultured 3T3-L1 adipocytes is unclear. OBJECTIVE: We investigated the action of osthole and its potential mechanisms in lipopolysaccharide (LPS)-stimulated 3T3-L1 adipocytes. MATERIALS AND METHODS: The 3T3-L1 adipocytes stimulated with LPS were cultured and treated with different concentrations of osthole. The inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cultured supernatants were detected by the enzyme-linked immunosorbent assay (ELISA) method, and the protein expressions of PPARα/γ and NF-κB p65 in adipocytes were detected by the Western blot method, respectively. RESULTS: Following treatment of adipocytes with osthole 0.1-1.6 µM, the TNF-α and IL-6 levels in cultured supernatants were decreased, and the NF-κB p65 protein expression in adipocytes was also decreased, while the PPARα/γ protein expressions were increased. After pretreatment of adipocytes with specific inhibitor(s) of PPARα and /or PPARγ, the inhibitory effects of osthole on TNF-α and IL-6 were decreased or almost cancelled, and the effects on NF-κB p65 protein expression also exhibited similar variations. CONCLUSION: Osthole could inhibit the TNF-α and IL-6 production in LPS-stimulated adipocytes, and its mechanism might be related to reduction of NF-κB expression via activation of PPARα/γ.

Content-illumination coupling guided low-light image enhancement network.

Current low-light enhancement algorithms fail to suppress noise when enhancing brightness, and may introduces structural distortion and color distortion caused by halos or artifacts. This paper proposes a content-illumination coupling guided low-light image enhancement network (CICGNet), it develops a truss topology based on Retinex as backbone to decompose low-light image component in an end-to-end way. The preservation of content features and the enhancement of illumination features are carried out along with depth and width direction of the truss topology. Each submodule uses the same resolution input and output to avoid the introduction of noise. Illumination component prevents misestimation of global and local illumination by using pre- and post-activation features at different depth levels, this way could avoid possible halos and artifacts. The network progressively enhances the illumination component and maintains the content component stage-by-stage. The proposed algorithm demonstrates better performance compared with advanced attention-based low-light enhancement algorithms and state-of-the-art image restoration algorithms. We also perform extensive ablation studies and demonstrate the impact of low-light enhancement algorithm on the downstream task of computer vision. Code is available at: https://github.com/Ruini94/CICGNet .

Robust internal model control based on a novel generalized extended state observer and its application on a two-inertia system.

Disturbance observer (DOB) and extended state observer (ESO) are extensively utilized to handle external disturbances and model uncertainties in the control system. Nevertheless, the integration of these two methods to improve disturbance suppression remains an open question. In this research, the disturbance compensation mechanism of DOB is employed to compensate the disturbance estimation error of ESO, thereby achieving an effective integration of DOB and ESO. Additionally, a generalized ESO (GESO) is proposed to replace ESO. A robust internal mode control (RIMC) scheme is then developed by incorporating GESO into a two-degree-of-freedom internal mode control (TDF-IMC) framework. Moreover, the equivalence of RIMC and classical TDF-IMC is given by a rigorous derivation under the frequency domain description. Finally, the RIMC is applied to the control of a two-inertia system to verify its superiority in terms of robustness, disturbance rejection, and resonance suppression.

Osthole regulates TGF-ß1 and MMP-2/9 expressions via activation of PPARα/γ in cultured mouse cardiac fibroblasts stimulated with angiotensin II.

PURPOSE: Our previous studies have demonstrated that osthole, an active constituent isolated from the fruit of Cnidium monnieri (L.) Cusson, can prevent isoprenaline-induced myocardial fibrosis in mice, but the underlying mechanism is still unclear. METHODS: The mouse cardiac fibroblasts (CFs) stimulated with angiotensin II (Ang II) were cultured and treated with different concentrations of osthole. The mRNA expressions of peroxisome proliferator-activated receptor (PPAR) α/γ, transforming growth factor ß1 (TGF-ß1), and matrix metalloproteinase (MMP)-2/9 were detected by reverse transcription polymerase chain reaction method, and the protein expressions of nuclear factor-κB (NF-κB) and TGF-ß1 were detected by Western blot method, respectively. RESULTS: Following treatment of cells with osthole at 2.5, 5, 10 and 20 µg/mL, the NF-κB and TGF-ß1 expressions were dose-dependently decreased, while the expressions of PPARα/γ and MMP-2/9 were dose-dependently increased. After the cells were preincubated with PPARα antagonist (MK886) or/and PPARγ antagonist (GW9662), the inhibitions of osthole on the NF-κB and TGF-ß1 expressions were decreased or completely halted and the increment of osthole on the MMP-2/9 expressions were also decreased or completely cancelled. CONCLUSION: Osthole could inhibit the NF-κB and TGF-ß1 expressions by activation of PPARα/γ, and subsequently enhance the MMP-2/9 expressions in cultured CFs, and these effects of osthole may play the beneficial roles in the prevention and treatment of myocardial fibrosis.

Exploring the potential molecular mechanism of trastuzumab-induced cardiotoxicity based on RNA sequencing and bioinformatics analysis.

The cardiotoxicity of trastuzumab (TRZ) seriously affects the prognosis of breast cancer patients, but the underlying mechanisms remains to be elucidated. This study aimed to investigate the potential molecular mechanisms of TRZ-induced cardiotoxicity based on RNA sequencing (RNA-Seq) and bioinformatics analysis. Kunming mice were exposed to 10 mg/kg TRZ for 6 and 10 days, followed by echocardiography, histopathology and serum biochemical analysis to evaluate the cardiotoxicity model. The results showed no significant changes after 6 days administration of TRZ. After 10 days administration of TRZ, the mice showed cardiac dysfunction, myocardial injury and fibrosis, and the serum levels of LDH, CK, CK-MB and cTnI were increased compared to the control [CON (Day 10)] group, indicating the cardiotoxicity model was successfully established. We compared gene expression levels in mice cardiac tissues by RNA-Seq and screened out 593 differentially expressed genes (DEGs). Results based on Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, protein-protein interaction (PPI) network analysis and RT-PCR revealed that the CD74/STAT1 signaling pathway might play an important role in TRZ-induced cardiotoxicity. In the TRZ group, the protein expressions of CD74, p-STAT1 (Tyr) and p-STAT1 (Ser) were increased. The TUNEL staining showed increased apoptosis of cardiomyocytes. In addition, an increased expressions of Bax, Caspase-3, IFN-γ and TNF-α and a decreased expression of Bcl-2 were observed in Western blot results, indicating the apoptosis and inflammation levels were increased. These findings suggested that TRZ may induce cardiotoxicity in mice by activating the CD74/STAT1 signaling pathway, which might be related to the induction of apoptosis and inflammation.